Effect of ventilation on acid-base balance and oxygenation in low blood- flow states

A. H. Idris, E. D. Staples, D. J. O'Brien, R. J. Melker, W. J. Rush, K. D. Del Duca, J. L. Falk

Research output: Contribution to journalArticle

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Abstract

Objectives: To investigate how minute ventilation affects the partial pressure of end-tidal CO2 and arterial and mixed venous pH, PCO2, PO2, and the concentration of bicarbonate during low blood-flow states. We tested the null hypothesis that acid-base conditions during low rates of blood flow are not significantly different when minute ventilation is doubled or halved. Design: Prospective, experimental, animal study. Setting: University hospital laboratory. Subjects: Domestic swine. Interventions: We studied ten anesthetized and mechanically ventilated swine (weight, 43 to 102 kg) in a new model of controlled systemic and pulmonary blood flow in which each animal was maintained on ventricular assist devices. After electrical induction of ventricular fibrillation, ventricular assist device blood flow was decreased in steps. At each decrease, control minute ventilation, two times the control minute ventilation (hyperventilation), and one-half the control minute ventilation (hypoventilation) were administered; each ventilatory change was maintained for 6 mins. Measurements and Main Results: Aortic, pulmonary arterial and central venous pressures, ventricular assist device blood flow, and end-tidal CO2 were recorded continuously. Acid-base conditions were studied at three different mean blood flow rates: 49%, 30%, and 12% of baseline prearrest cardiac index. Arterial pH and PaO2 and mixed venous pH varied directly (p < .003) with minute ventilation, while PaCO2 and mixed venous PCO2, and end-tidal CO2 varied inversely (p < .0001) with minute ventilation. Mixed venous PO2 was not significantly related to minute ventilation (p = .6). PaCO2 and arterial bicarbonate; mixed venous pH, mixed venous PO2, and mixed venous bicarbonate, and end-tidal CO2 varied directly (p < .001) with blood flow, while mixed venous PCO2 varied inversely with blood flow (p < .05). Arterial pH was not significantly related to blood flow (p = .3). When minute ventilation changed from hyperventilation to hypoventilation at a mean blood flow rate of 49%, mean arterial pH decreased 0.22 ± 0.06 (p < .05), mean PaCO2 increased 28 ± 6 torr (3.7 ± 0.8 kPa) (p < .05), and mean PaO2 decreased 99 ± 77 torr (13.2 ± 10 kPa); mean mixed venous pH decreased 0.11 ± 0.02, mean mixed venous PCO2 increased 16 ± 2.2 torr (2.1 ± 0.3 kPa) (p < .05), and mean mixed venous PO2 did not change; mean end-tidal CO2 increased 18 ± 2 torr (2.4 ± 0.3 kPa) (p < .05). The effect of changes in minute ventilation on blood gases and end- tidal CO2 was similar for mean blood flow rates of 30% and 12% of baseline cardiac index. Conclusions: During low rates of blood flow similar to those rates found in shock and cardiopulmonary resuscitation, alterations in minute ventilation significantly influenced end-tidal CO2 and both arterial and mixed venous pH and PCO2. These findings may have clinical importance in improving the treatment of shock and cardiac arrest.

Original languageEnglish (US)
Pages (from-to)1827-1834
Number of pages8
JournalCritical Care Medicine
Volume22
Issue number11
StatePublished - 1994

Fingerprint

Acid-Base Equilibrium
Ventilation
Heart-Assist Devices
Hyperventilation
Bicarbonates
Shock
Swine
Hospital Laboratories
Lung
Central Venous Pressure
Acids
Partial Pressure
Cardiopulmonary Resuscitation
Ventricular Fibrillation
Heart Arrest
Research Design

Keywords

  • acid-base equilibrium
  • acidosis
  • alkalosis
  • blood gas analysis
  • cardiac output
  • fibrillation
  • hemodynamics
  • mechanical ventilation
  • pH
  • resuscitation

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Idris, A. H., Staples, E. D., O'Brien, D. J., Melker, R. J., Rush, W. J., Del Duca, K. D., & Falk, J. L. (1994). Effect of ventilation on acid-base balance and oxygenation in low blood- flow states. Critical Care Medicine, 22(11), 1827-1834.

Effect of ventilation on acid-base balance and oxygenation in low blood- flow states. / Idris, A. H.; Staples, E. D.; O'Brien, D. J.; Melker, R. J.; Rush, W. J.; Del Duca, K. D.; Falk, J. L.

In: Critical Care Medicine, Vol. 22, No. 11, 1994, p. 1827-1834.

Research output: Contribution to journalArticle

Idris, AH, Staples, ED, O'Brien, DJ, Melker, RJ, Rush, WJ, Del Duca, KD & Falk, JL 1994, 'Effect of ventilation on acid-base balance and oxygenation in low blood- flow states', Critical Care Medicine, vol. 22, no. 11, pp. 1827-1834.
Idris AH, Staples ED, O'Brien DJ, Melker RJ, Rush WJ, Del Duca KD et al. Effect of ventilation on acid-base balance and oxygenation in low blood- flow states. Critical Care Medicine. 1994;22(11):1827-1834.
Idris, A. H. ; Staples, E. D. ; O'Brien, D. J. ; Melker, R. J. ; Rush, W. J. ; Del Duca, K. D. ; Falk, J. L. / Effect of ventilation on acid-base balance and oxygenation in low blood- flow states. In: Critical Care Medicine. 1994 ; Vol. 22, No. 11. pp. 1827-1834.
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abstract = "Objectives: To investigate how minute ventilation affects the partial pressure of end-tidal CO2 and arterial and mixed venous pH, PCO2, PO2, and the concentration of bicarbonate during low blood-flow states. We tested the null hypothesis that acid-base conditions during low rates of blood flow are not significantly different when minute ventilation is doubled or halved. Design: Prospective, experimental, animal study. Setting: University hospital laboratory. Subjects: Domestic swine. Interventions: We studied ten anesthetized and mechanically ventilated swine (weight, 43 to 102 kg) in a new model of controlled systemic and pulmonary blood flow in which each animal was maintained on ventricular assist devices. After electrical induction of ventricular fibrillation, ventricular assist device blood flow was decreased in steps. At each decrease, control minute ventilation, two times the control minute ventilation (hyperventilation), and one-half the control minute ventilation (hypoventilation) were administered; each ventilatory change was maintained for 6 mins. Measurements and Main Results: Aortic, pulmonary arterial and central venous pressures, ventricular assist device blood flow, and end-tidal CO2 were recorded continuously. Acid-base conditions were studied at three different mean blood flow rates: 49{\%}, 30{\%}, and 12{\%} of baseline prearrest cardiac index. Arterial pH and PaO2 and mixed venous pH varied directly (p < .003) with minute ventilation, while PaCO2 and mixed venous PCO2, and end-tidal CO2 varied inversely (p < .0001) with minute ventilation. Mixed venous PO2 was not significantly related to minute ventilation (p = .6). PaCO2 and arterial bicarbonate; mixed venous pH, mixed venous PO2, and mixed venous bicarbonate, and end-tidal CO2 varied directly (p < .001) with blood flow, while mixed venous PCO2 varied inversely with blood flow (p < .05). Arterial pH was not significantly related to blood flow (p = .3). When minute ventilation changed from hyperventilation to hypoventilation at a mean blood flow rate of 49{\%}, mean arterial pH decreased 0.22 ± 0.06 (p < .05), mean PaCO2 increased 28 ± 6 torr (3.7 ± 0.8 kPa) (p < .05), and mean PaO2 decreased 99 ± 77 torr (13.2 ± 10 kPa); mean mixed venous pH decreased 0.11 ± 0.02, mean mixed venous PCO2 increased 16 ± 2.2 torr (2.1 ± 0.3 kPa) (p < .05), and mean mixed venous PO2 did not change; mean end-tidal CO2 increased 18 ± 2 torr (2.4 ± 0.3 kPa) (p < .05). The effect of changes in minute ventilation on blood gases and end- tidal CO2 was similar for mean blood flow rates of 30{\%} and 12{\%} of baseline cardiac index. Conclusions: During low rates of blood flow similar to those rates found in shock and cardiopulmonary resuscitation, alterations in minute ventilation significantly influenced end-tidal CO2 and both arterial and mixed venous pH and PCO2. These findings may have clinical importance in improving the treatment of shock and cardiac arrest.",
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TY - JOUR

T1 - Effect of ventilation on acid-base balance and oxygenation in low blood- flow states

AU - Idris, A. H.

AU - Staples, E. D.

AU - O'Brien, D. J.

AU - Melker, R. J.

AU - Rush, W. J.

AU - Del Duca, K. D.

AU - Falk, J. L.

PY - 1994

Y1 - 1994

N2 - Objectives: To investigate how minute ventilation affects the partial pressure of end-tidal CO2 and arterial and mixed venous pH, PCO2, PO2, and the concentration of bicarbonate during low blood-flow states. We tested the null hypothesis that acid-base conditions during low rates of blood flow are not significantly different when minute ventilation is doubled or halved. Design: Prospective, experimental, animal study. Setting: University hospital laboratory. Subjects: Domestic swine. Interventions: We studied ten anesthetized and mechanically ventilated swine (weight, 43 to 102 kg) in a new model of controlled systemic and pulmonary blood flow in which each animal was maintained on ventricular assist devices. After electrical induction of ventricular fibrillation, ventricular assist device blood flow was decreased in steps. At each decrease, control minute ventilation, two times the control minute ventilation (hyperventilation), and one-half the control minute ventilation (hypoventilation) were administered; each ventilatory change was maintained for 6 mins. Measurements and Main Results: Aortic, pulmonary arterial and central venous pressures, ventricular assist device blood flow, and end-tidal CO2 were recorded continuously. Acid-base conditions were studied at three different mean blood flow rates: 49%, 30%, and 12% of baseline prearrest cardiac index. Arterial pH and PaO2 and mixed venous pH varied directly (p < .003) with minute ventilation, while PaCO2 and mixed venous PCO2, and end-tidal CO2 varied inversely (p < .0001) with minute ventilation. Mixed venous PO2 was not significantly related to minute ventilation (p = .6). PaCO2 and arterial bicarbonate; mixed venous pH, mixed venous PO2, and mixed venous bicarbonate, and end-tidal CO2 varied directly (p < .001) with blood flow, while mixed venous PCO2 varied inversely with blood flow (p < .05). Arterial pH was not significantly related to blood flow (p = .3). When minute ventilation changed from hyperventilation to hypoventilation at a mean blood flow rate of 49%, mean arterial pH decreased 0.22 ± 0.06 (p < .05), mean PaCO2 increased 28 ± 6 torr (3.7 ± 0.8 kPa) (p < .05), and mean PaO2 decreased 99 ± 77 torr (13.2 ± 10 kPa); mean mixed venous pH decreased 0.11 ± 0.02, mean mixed venous PCO2 increased 16 ± 2.2 torr (2.1 ± 0.3 kPa) (p < .05), and mean mixed venous PO2 did not change; mean end-tidal CO2 increased 18 ± 2 torr (2.4 ± 0.3 kPa) (p < .05). The effect of changes in minute ventilation on blood gases and end- tidal CO2 was similar for mean blood flow rates of 30% and 12% of baseline cardiac index. Conclusions: During low rates of blood flow similar to those rates found in shock and cardiopulmonary resuscitation, alterations in minute ventilation significantly influenced end-tidal CO2 and both arterial and mixed venous pH and PCO2. These findings may have clinical importance in improving the treatment of shock and cardiac arrest.

AB - Objectives: To investigate how minute ventilation affects the partial pressure of end-tidal CO2 and arterial and mixed venous pH, PCO2, PO2, and the concentration of bicarbonate during low blood-flow states. We tested the null hypothesis that acid-base conditions during low rates of blood flow are not significantly different when minute ventilation is doubled or halved. Design: Prospective, experimental, animal study. Setting: University hospital laboratory. Subjects: Domestic swine. Interventions: We studied ten anesthetized and mechanically ventilated swine (weight, 43 to 102 kg) in a new model of controlled systemic and pulmonary blood flow in which each animal was maintained on ventricular assist devices. After electrical induction of ventricular fibrillation, ventricular assist device blood flow was decreased in steps. At each decrease, control minute ventilation, two times the control minute ventilation (hyperventilation), and one-half the control minute ventilation (hypoventilation) were administered; each ventilatory change was maintained for 6 mins. Measurements and Main Results: Aortic, pulmonary arterial and central venous pressures, ventricular assist device blood flow, and end-tidal CO2 were recorded continuously. Acid-base conditions were studied at three different mean blood flow rates: 49%, 30%, and 12% of baseline prearrest cardiac index. Arterial pH and PaO2 and mixed venous pH varied directly (p < .003) with minute ventilation, while PaCO2 and mixed venous PCO2, and end-tidal CO2 varied inversely (p < .0001) with minute ventilation. Mixed venous PO2 was not significantly related to minute ventilation (p = .6). PaCO2 and arterial bicarbonate; mixed venous pH, mixed venous PO2, and mixed venous bicarbonate, and end-tidal CO2 varied directly (p < .001) with blood flow, while mixed venous PCO2 varied inversely with blood flow (p < .05). Arterial pH was not significantly related to blood flow (p = .3). When minute ventilation changed from hyperventilation to hypoventilation at a mean blood flow rate of 49%, mean arterial pH decreased 0.22 ± 0.06 (p < .05), mean PaCO2 increased 28 ± 6 torr (3.7 ± 0.8 kPa) (p < .05), and mean PaO2 decreased 99 ± 77 torr (13.2 ± 10 kPa); mean mixed venous pH decreased 0.11 ± 0.02, mean mixed venous PCO2 increased 16 ± 2.2 torr (2.1 ± 0.3 kPa) (p < .05), and mean mixed venous PO2 did not change; mean end-tidal CO2 increased 18 ± 2 torr (2.4 ± 0.3 kPa) (p < .05). The effect of changes in minute ventilation on blood gases and end- tidal CO2 was similar for mean blood flow rates of 30% and 12% of baseline cardiac index. Conclusions: During low rates of blood flow similar to those rates found in shock and cardiopulmonary resuscitation, alterations in minute ventilation significantly influenced end-tidal CO2 and both arterial and mixed venous pH and PCO2. These findings may have clinical importance in improving the treatment of shock and cardiac arrest.

KW - acid-base equilibrium

KW - acidosis

KW - alkalosis

KW - blood gas analysis

KW - cardiac output

KW - fibrillation

KW - hemodynamics

KW - mechanical ventilation

KW - pH

KW - resuscitation

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